The present research has demonstrated that environmental stressors acting during prenatal but not postnatal development, feminize and demasculinize a variety of sexually dimorphic behaviors in male rats, including ejaculatory and lordotic patterns. This complex of changes has been called the prenatal stress syndrome. The sexual behavior of pre and/or postnatally stressed females is not altered. It is postulated that prenatal stress reduces the amount of androgen released by the fetal testes. Since androgen is needed during fetal development to organize the sexual behavior patterns characteristic of normal males, stress-induced attenuation of androgen will result in feminization and demasculinization of behavior. It is one objective of this proposal to test this theory directly. Plasma, testosterone, progesterone, and corticosterone titers of stressed and control fetal males and their female littermates will be measured by radioimmunoassay during the stages in perinatal development in which sexual behavior differentiates. Also a more detailed appraisal of the nature of the deficit in ejaculatory behavior will be made through adult androgen treatment, intracranial implantation of sodium testosterone sulfate, and exposure to further stress in adulthood. The possible causes of within litter variability will be probed and the interaction of prenatal stress with prepubertal socializing experiences assessed. We plan to extend the generality of this syndrome to species other than the rat and to stressors other than light and restraint. Finally, we will investigate the extent to which the mothers and fetuses adapt to the stress procedure and thus, possibly, minimize the potential impact of prenatal stress on sexual differentiation.